1188-38-1
1188-38-1 结构式
基本信息
卡哥鲁酸
氨甲酰谷氨酸
N-氨甲酰基谷氨酸
N-氨基甲酰谷氨酸
N-氨甲酰-L-谷氨酸
N-氨基甲酰-L-谷氨酸
N-氨基甲酰基-L-谷氨酸
N-氨基甲酰谷氨酸(NCG)
N-氨基甲酰-L-谷氨酸(N-氨甲酰-L-谷氨酸)
Carbaglu
N-Cbm-Glu-OH
carglumicaci
CargluMic Acid
ureidoglutaricacid
n-carbamylglutamate
carbamylglutamicacid
N-Carbamyl-L-glutamic
N-Carbamyl-L-glutamate
物理化学性质
安全数据
制备方法
590-28-3
56-86-0
1188-38-1
以氰酸钾和L-谷氨酸为原料合成N-氨基甲酰-L-谷氨酸的一般步骤如下：将4 mmol的L-谷氨酸溶解于20 mL水中，使用浓盐酸（37 μL，体积分数）酸化该溶液。随后，向酸化后的溶液中加入12 mmol的硫氰酸钾（KOCN）。在持续搅拌下，将反应混合物加热至333 K，维持此温度反应4小时。反应完成后，将溶液冷却至室温，并转移至用封口膜密封的玻璃小瓶中，封口膜上穿孔以促进溶剂蒸发，直至观察到白色固体析出。通过缓慢蒸发乙醇溶液的方法，在室温下培养出适合X射线单晶衍射分析的（I）晶体（参见方案1）。该合成方法的产率为62%，所得产物的熔点为170°C至171°C。此实验步骤是对先前报道方法的改进和优化。
参考文献：
[1] Molecular Crystals and Liquid Crystals, 2016, vol. 625, # 1, p. 225 - 232
[2] Pharmaceutical Chemistry Journal, 1978, vol. 12, # 5, p. 601 - 606
[3] Khimiko-Farmatsevticheskii Zhurnal, 1978, vol. 12, # 5, p. 53 - 59
常见问题列表
CPS1
Carglumic acid suppresses cell viability in the pancreatic ductal adenocarcinoma cell lines, triple-negative breast cancer cell lines, hepatoma cell lines, and human non-small cell lung carcinoma cell lines in a dose-dependent manner. The 50% inhibitory concentration (IC 50 ) of Carglumic acid against those cell lines is between 5 and 7.5 mM. The results show that Carglumic acid does not induce complete cell cycle arrest. Instead, there are more sub-G1 cells among Carglumic acid-treated AsPC1 and MDA-MB-231 cells than among untreated cells. In AsPC1 and HPDE-E6E7 cells, the IC 50 s of Carglumic acid are 5 mM and over 10 mM, respectively . In MDA-MB-231 and MCF-12A cells, the IC 50 s of Carglumic acid are 5 mM and 6 mM, respectively.
The results show that Carglumic acid, but not the vehicle control, markedly inhibits tumor growth. In the orthotopic pancreatic cancer model, tumor growth inhibition by Carglumic acid on day 21 is 80% (P<0.01). In the orthotopic triple-negative breast cancer model, tumor growth inhibition by Carglumic acid on day 20 is 82% (P<0.01). These results indicate that Carglumic acid suppresses tumor growth in pancreatic cancer and triple-negative breast cancer. On day 20, mean tumor growth inhibition in orally and intravenously treated mice is 55% and 93%, respectively, relative to untreated mice (P<0.01).